Lecture 16 Flashcards
NZ nutrient reference values
Nation health Medical research council Australia
Derived from different methods - e.g. prisoner of war camps (Balance Studies: people deficient in specific nutrients, symptoms, feed w nutrients to determine amount of nutrients required for optimum health). Animal studies. Factorial analysis
1. Bell shaped curve/Gulcatian distribution - normal nutrient requirement for population by age and sex
2. Estimated average requirement - peak of bell curve/half way point
3. RDI - 2x standard deviations from mean - covers 98% of population requirement - nutrient serving basis
Derivation of Nutrient reference values
Derived from different methods - e.g. prisoner of war camps (Balance Studies: people deficient in specific nutrients, symptoms, feed w nutrients to determine amount of nutrients required for optimum health). Animal studies. Factorial analysis
- Hard to get true indication of an individual nutrient’s requirement, as if remove one nutrient from diet often removing whole food group, leading to removal of other nutrients.
- Nutrient Reference values are the best guestemate
NRV
Naive: black and white view
Reality: Adequate intake. Margin of safety more/less than RDI. Danger/Likelihood of toxicity or deficiency . Have a more variable response to nutrients, not black and white.
Water soluble Vitamins
- Vitamin C (ascorbic acid)
- Thiamin (vit B1)
- Riboflavin (vit B2)
- Niacin (vit B3)
- Pantothenic acid (vit B5)
- Pyridoxine (vit B6)
- Cobalamin (vit B12)
- Folate (folic acid)
- Biotin
Fat soluble Vitamins
DrAKE
- vit D (cholecalciferol)
- vit A (retinol, carotenes)
- vit K (phylloquinone, menaquinone, menadione)
- vit E (tocopherols and tocotrienes)
Water soluble Vit C and B role in body
Absroption SI, Directly into blood
Travel freely (in blood)
Circulate freely in water-filled parts of the body (within cells)
Kidneys detect and remove excess urine (after saturating/requirement for them) (exrete whole gram of boroca)
Possible to reach toxic levels when consumed from supplements
Needed in frequent doses (perhaps 1-3 days) (need to consume requrally as dont store them)
Fat soluble Vit A, D, E and K role in body
Absrobed (with Fat (as fat-soluble) First into lymph then –> into blood
Many require protein carriers (through blood)
Stored in the cells associated with fat
Less readily excreted, tend to remain in fat storage sites (only excrete once fat is turned over/utilised for energy production)
Likely to reach toxic levels when consumed from supplements
Needed in periodic doses (perhaps weeks or even months)
-stored so protected from deficiency relatively more
6x Factors affecting bioavailbility
- Efficiency of digestion/transit time (imparied fat absoprtion/fat malabsorption)
- Previous nutrient intake and nutritional status
- Other foods consumed simultaneously (when eating dont consume single nutrients, nutrients fit within food matrix, effects how bioavailble nutrients are at gut level)
- Food preparation method (dont boil brocolli in water for a long time, Vit C and folate into water. These vitamins easily oxidised/destroyed after long periods of time)
- Source of nutrient - synthetic or natural. supplements biovaolity vs food chemical viatmin form.
- Health status
B vitamins Names and Functions
- Metabolism (fat carb and protein) of energy yielding intermediates via red/ox reactions
Thiamin B1
Riboflavin B2
Niacin B3 - Pyridoxin B6 Transamination (aa metabolism)
- Cobalamin B12 Transmethylation
Folate B9 - Constituents: energy metbaolism
Panthothenic acid B5 Constituent of co-enzyme A
Biotin B7 Carboxylation using coenzyme A (carbox cycle)
Breaking down nutrients for energy
all enter into TCA cycle
most involve B factors as co-enzymes (converting fat–> pyruvate –>acetyl A and a/acids)
Thiamine’s involvement in metabolic pathway
Metabolic conversion
TPP - triparaphosphate
3x coenzyme functions in metbaolism
1. Glucose pathway: Conversion of Pyruvate –> Acetyl co-enzyme A
2. TCA cycle: branch chain a/acid 3. conversion of Keto-acids
-therefore if you have a deficiency in B vitamins, will have effect a large number of systems.
-ability to produce energy
-ability to produce specific a/acids (for neuroregulation, modulation, homrone production, specific protein production)
Deficiency in B vitamins
effect a large number of systems.
- ability to produce energy
- ability to produce specific a/acids (for neuroregulation, modulation, hormone production, specific protein production)
Thiamine deficiency
Beriberi=sheep-wobbly, bowed legs, mental affected.
Endemic in population in milled/white rice populations(nut husk nutrients). Prisons in small diets
-shows how thiamine is involved in so many body systems
1. Wet Beriberi: Cardiovascular disease of thiamine deficiency
-Swelling (oedema)- pooling in ECF in Extracellular spaces
-increased heart rate (tachycardia)
-lung congestion (poor circulation, pooling of extracellular fluid odema)
-congestive heart failure.
Lower extremeities and face swollen. Press with thumb for period of time- forms “pitting”
2. Dry Beriberi: Neurological disease of thiamine deficiency- can do exist with wet beriberi
-pain, tingling or loss of sensation in hands and feet (peripheral neuropathy)
-muscle wasting with loss of function of lower extremities
-dermititis in knees and elbow
-brain damage
-death
3. Infant Beriberi
Causes of Thiamine deficiency
Alcoholism is main cause of thiamin deficiency in western world
- thiamine involved in carb metabolism and alcohol dehydrogenase/alcohol removal within liver
- Alcoholism and Thiamine deficiency is the main preventable causes of neurological problems
- try to put thiamine in beer
- TreatmentThiamine replacement treatment therapy
- signs and symptoms can be reversable to a certain degree (and some brain damage may still occur) -dependant on amount of brain damage that has occurred
1. Wernicke-encephalopathy - alcohol related brain damage - language problems (difficulty moving), walking difficulty, unusual eye movement (also seen in people with starvation)
2. Korsakoff Syndrome - amnesia, inability to learn, confabulation
Wernicke Enchepalopathy
alcohol related brain damage - language problems (difficulty moving),
walking difficulty,
unusual eye movement (also seen in people with starvation)
-thiamine involved in carb metabolism and alcohol dehydrogenase/alcohol removal within liver
-Alcoholism and Thiamine deficiency is the main preventable causes of neurological problems
Korsakoff Syndrome
amnesia,
inability to learn,
confabulation
-thiamine involved in carb metabolism and alcohol dehydrogenase/alcohol removal within liver
-Alcoholism and Thiamine deficiency is the main preventable causes of neurological problems
Folate
Ring structure + Glutamate(s)
-vitally important for production of DNA and therefore new cells (interaction with B12, methyl donation for DNA production. % methyl THF and THF, w assistance of Methyl group from B12 (cycle of methionine from homocysteine, produces methyl group that can be donated for DNA production)
In foods, folate naturally occurs as a polyglutamates (spinach)
-Folate occurs as mono-glutamate in fortified foods and supplements
In the intestine, digestion breaks glutamates off and adds a methyl group. Folate is absorbed and delivered to cells
-required in enteric absorption of folate, otherwise isnt absorbed
- low folate levels same as B12 deficiency due to close association, hard to differentiate between
Folate deficiency
- low folate levels same as B12 deficiency due to close association, hard to differentiate between
1. Megaloblastic anaemia (large, disordered shaped red cells)- same as B12
2. Neural Tube defects (NTDs) during fetal developments e.g. spinal bifida - inability of spinal cord not closed off - born with some spinal cord not covered and exposed to external body
- leads to paralysis of lower limbs.
- variable disability depending on nerual tube defect severity
3. ? elevated risk of cancer and heart disease and mental abnormalities - due to methylation pathway when producing homocysteine
- people with low levels of homocystine (especially if have specific genetic variants) have increased risk of CVD
Main causes of Folate deficiency
- Low dietary intake (green leafy veges, oranges)
- Reduced intestine absorption (sprue and coeliac disease, SI inflammatory disease)
- Anticonvulsant drugs; some lipid lowering drugs
- Folate antagonises - methotrexate (cancer treamtnets. Interfere with folate metbaolism)
- High alcohol intake- leading to decreased absorption, increased catabolism, often accompanied by poor diet
- Pregnancy (and offspring) - due to increased folate requirement during pregnancy, more needed to produce new cells for fetus to grow
Requirement of Folate during pregnancy
Weeks gestation from LMP (last mentral period) - most susceptible time for major malformation
We are currently intervening too late. Critical periods of development:
CNS: 5-8 early period. if folate deficient, can impact fetus CNS development
Heart 5-8
Arms: 6-10
Eyes 6-10
Legs 6-9
Teeth 8-10
Palate 8-11
External genetalia 9-11
Ear 6-11
Woman should take folate supplement 4 weeks before pregnancy, and continue for first 12 weeks/first rimester of pregnancy
-to prevent neural tube defects
-NZ neural tube defects 12-14 infant per 10,000 (no fortification. only supplementation/voluntary code)
-other countries with mandatory fortification of folate food supply, 7-9 per 10,000 (Aus flour, Uk and US)
-high correlation with neural tube defects incidence and level of country’s folate food fortification
Ministry of Health Folic acid in Pregnancy
800ug/day 4 weeks prior to 12 weeks (first trimester of prengnacy)
Family history of neural tube defects/had previous child with neural tube defect - recommended 5000ug/day previous history
Subsadised by Pharmac for pregnant woman
-Problem: assuming all pregnancies were planned approx 40% of pregnancies unplanned in NZ.
- by time found out pregnant, may have missed first 12wk trimester. Too late to effect development of CNS (and hence spinal cord)
Folic acid use during 3 months before pregnancy by pregnancy planning
Pregnancy planned for 60%
Planned pregnancy - 58% used folate during 3 months before pregnancy
(significant number still without sufficient folate supplemention even though planned)
Unplanned pregnancy -9%
-continued with children until 5 years old.
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Vitamin A and Beta Carotene
Fat soluble vitamins most likely food deficiencies/toxicity
In foods/diet:
1. Retinyl esters - in animal foods –> retinol (supports reproduction)
2. Beta-carotene - in plant foods (can participate in Vit A metabolic functions) –> Retinal (participates in vision) (conversion between retinol and retinal) —> Retinal can be converted to retinoic acid (regulates growth)
Vitmain A and Vision
Retinal from plant foods/Beta Carotene
As light enters the eye (cornea), pigments within the cells of the retina absorb the light
The cells (rods and cones) of the retina contain rhodopsin, a molecule composed of opsin ( a protein) and cis-retinal (vit A)
As rhodopsin absorbs light, rhodopsin splits, retinal changes from cis–> trans
-triggers a nerve impulse that carries visual information to the brain (so we can see light)
-w/o Vit A - impaired vision, especially poor night vision
Vitamin A and Protein synthesis/Cell differentiation
Vitamin A very important in cell differentiation
Mucous membranes have high turn over cells - and RBC and immune cells. all require vit A
-Vitamin A maintains healthy cells in the mucous membranes
-W/o vitamin A, the normal structure and function of the cells in the mucous membranes are impaired
-poor mucous membrane production
-poor turn over of cells in mucous membrane- lungs and gut
-more susceptible to infection
-endemic vit A deficiencies, when children given vaccines also given large intramuscular dose of Vit A - to ensure body can utilise immunisation effectively, to convert vaccine in body. If body Vitamin A replete, then immunisation worthless
Vitamin A Keratinisation symptom
tiny bumps on uneven skin surface
-poor immune response/high susceptibility to infection - distinguishable feature of Vit A deficiency
Vitamin A toxicity
Vit A fat soluble vitamin, therefore could cause toxicity
- Vit A (fat soluble) toxicity can cause severe liver damage
- Overconsumption from supplements/ Anti-acni medication which is predominantly retinal - Beta carotene (water soluble therefore harder to reach toxity)
- found in many fruits and veges
- Inefficient conversion
- Overconsumption from food - yellow skin (common in young children/toddles. Like sweet vege , and comes in numerous forms) - face and palsm fo hands. Not dangerous, and is reversible/not longterm)
Vitamin D
could argue vit D isnt nutrient, as main way of manufacturing vit D is from sunlight, and behaves alot like a hormone in body
-Calciferol
-1,25 dihyrdoxy cit D (calcitrol)- metbaolically active form. can be prescribed
Animal version : vit D3 or cholecalciferol
Plant version: Vit D2 or Ergocelciferol
-few animal or plant sources as good Vit D, more sunlight
Precursor is the bodys own cholestrol
Vitamin D from sunlight
- In the skin
-needs to be certain UV wavelength and height to manufacture Vit D in skin (NZ north-9 months + south-6 months)
-7-dehydrocholestrol ( a precursor made in the liver from cholestrol) —Ultraviolet light from the sun –> Previtamin D3 (some D3 and D2 from diet but v small as no fortification mandatory of food supply)– + Foods –> Vitamin D3 (an inactive form) - In the liver
–Hydroxylation –> 25-hydroxy vitamin D3 - In the Kidneys
–Hydroxylation –> 1, 25 hydroxy vitamin D3 (active form-to be metabolically active in body)
Effective supplements need to be Hydroxylated forms of Vitamin D (1,25 hydroxy vitamin D3)
Vitamin D supplements
Need to be Hydroxylated forms of Vitamin D (1,25 hydroxy vitamin D3)
Food sources of Vitamin D
require around 400 IU (international units) daily Cod liver oil - 1tbps = 1360 IU Salmon, cooked - 100g = 360 IU Milk (fortified. Anlene) - 250ml =260 IU Sardines in oil -100g = 345 IU Beef Liver, cooked - 100g = 30 IU Mushrooms, raw - 1/2 cup =27 IU Egg - 1 whole = 20 IU
Vitamin D Bone mineralisation
- Sun
- Pre-vitamin D + skin
- Vitamin D (+ supplements and Salmon)
- Liver
- 25(OH)D
–> Prostate gland, breast, colon, lung immune cells
–> 1,25 (OH)2D
–> a) regulation of cell growth (cancer prevention)
–> b) Regulation of immune function (diabetes type 1,MS. RA autoimmune disease prevention)
-Vitamin D receptors are found on most cells of most organs in the body. Has an effect on many other regulation organs.
Research: large dose Vit. D supplementation?- impact on endocrine function (diabetes risk of at risk individuals), autoimmune disease prevention (muscular sclerosis) - Kidney
–> 1,25(OH)2D
–> Calcium, Muscle, Bone health & regulation of blood pressure Insulin production (heart disease and diabetes prevention)
-cannot absorb calcium without vitamin D. also important for reabsorption of calcium into bones
-Vitamin D hormone behaving,
Vitamin D by month 2002 : Nz children
Adjusted for age, sex, latitude, obesity and overweight
- change 31
- similar picture for adults
- seasonal levels. (recommended is 50 nmol/L in serum)
- spring/summer: median levels above 50
- dont know what this seasonal changes in vit D impact has on health status
- countries with mandatory fortification of Vit D in food products (eg. milk products, butters margarines)- big seasonal differences not seen (summer and winter vit D levels)
Vitamin D deficiency diseases
Vit d important in bone mineral deficiency –> results in poor bone formation
1. Rickets - children
Bowed legs - poorly formed long bones of the legs bend outwards as weight bearing activities such as walking began (cannot hold weight in legs)
-seen in recent migrants with darker skin. Darker skin takes longer to manufacture same amount of Vit D, due to darker pigemntation. cultures where cover body due to religion.
2. Osteomalacia - adults
Who needs Vitamin and Mineral Supplements?
Nz good supplement users.
People who have:
1. Poor nutrient intake (elderly, dieters (esp those house bound and dont get sunlight), adolescents, vegeterians (dont get all nutrients from balanced diet))
2. Increased nutrient requirements (children, pregnancy(folate)/lactation)
3. Increased metabolic demands (surgery/trauma/fracture)-feed people artificially/naso-gastrically or intravenously (particularily B vitamins increaed demand for energy)
4. Maldigestion or Malabsorption (liver disease, GI, diarrhea)
5. Drug-nutrient interactions (prednisone/Vit D, diuretics/K,Mg)- nutrient delivery may need to change
6. Medical treatment interactions (chemo/radiation) - over the counter preparations, herbal and dietary supplement use. Methotrexate in cancer treatment
7. Need from pharmacological disease (niacin for hyperlipidemia)- does prescribed much higher RDI nescessary
Percent regular supplement use, by age group and sex. Key findings of the 2008/09 NZ Adult nutrition survey
High regular use of dietary supplements.
